These authors contributed equally to this body of work.
Migration Inhibitory Factor Secretion by Polarized Uterine Epithelial Cells is Enhanced in Response to the TLR3 Agonist Poly (I:C)
Version of Record online: 31 AUG 2005
American Journal of Reproductive Immunology
Volume 54, Issue 4, pages 193–202, October 2005
How to Cite
Schaefer, T. M., Fahey, J. V., Wright, J. A. and Wira, C. R. (2005), Migration Inhibitory Factor Secretion by Polarized Uterine Epithelial Cells is Enhanced in Response to the TLR3 Agonist Poly (I:C). American Journal of Reproductive Immunology, 54: 193–202. doi: 10.1111/j.1600-0897.2005.00298.x
- Issue online: 31 AUG 2005
- Version of Record online: 31 AUG 2005
- Submitted March 11, 2005; revised May 18, 2005; accepted May 27, 2005.
- Epithelial cells;
- macrophage migration inhibitory factor;
- toll-like receptor 3;
Uterine epithelial cells produce cytokines that stimulate leukocytes in response to a microbial insult. The goals of this study were to determine if uterine epithelial cells produce the pro-inflammatory cytokine macrophage migration inhibitory factor (MIF), and to see if toll-like receptor (TLR) agonists stimulate MIF secretion.
Methods of study
Human uterine epithelial cells were isolated and grown in cell culture inserts. Levels of MIF secretion were examined by ELISA and MIF messenger RNA (mRNA) expression was examined using real time RT-PCR.
Uterine epithelial cells constitutively secrete MIF and exposure to the TLR3 agonist poly (I:C) resulted in enhanced apical secretion of MIF. MIF secretion appeared to be from pre-formed intracellular stores, since exposure of epithelial cells to poly (I:C) had little effect on the expression of MIF–mRNA.
These results demonstrate that uterine epithelial cells constitutively produce MIF and stimulation with poly (I:C) results in enhanced MIF production. This suggests that MIF secretion by uterine epithelial cells may play a critical role in innate immune responses against viral pathogens mediated through TLR3.